Asthma Flashcards

1
Q

Definition

A

Chronic inflammatory condition of the lung airways

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2
Q

3 characteristics of asthma

A

Airflow limitation
Airway hyperreponsiveness
Inflammation of the bronchi

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3
Q

Is airflow limitation reversible?

A

yes, usually spontaneously/with treatment

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4
Q

What cell types are involved in inflammation of the bronchi?

A
T lymphocytes
Mast cells
Eosinophils
Oedema
SM hypertrophy
Matrix deposition
Mucus plugging 
epithelial damage
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5
Q

What is extrinsic asthma

A

Atopic - implying a definite external cause

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6
Q

What is intrinsic asthma

A

when no causative agent can be identified - often ‘late onset’

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7
Q

Atopy

A

tendency to develop IgE antibody mediated reactions against environmental antigens

genetic and environmental factors affect serum IgE levels

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8
Q

What are bronchial provocation tests?

A

Patients inhale gradually increasing concentrations of either histamine or methacholine.

Patients with clinical Sx of asthma respond to very low doses

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9
Q

What is the eosinophilic asthma phenotype?

A

allergic, Th2

  • early onset, atopy associated
  • later onset, non-atopic
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10
Q

Which cells are jam packed with granules and have high affinity IgE receptors?

A

mast cells

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11
Q

What’s mast cell sensitisation?

A

when mast cells get IgE associated with its IgE receptors, and its then primed to be activated

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12
Q

What happens when a mast cell is activated?

A

it releases mediators and degranulates

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13
Q

3 mast cell mediators and what time frame are they released in?

A

Histamine seconds
Eicosanoids minutes
Cytokines hours

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14
Q

what is a very potent bronchoconstrictor?

A

histamine

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15
Q

What are cys-LT1 and cys-LT2?

A

cysteinyl-leukostrienes (a type of eicosanoid)

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16
Q

Precipitating factors for asthma

A
major allergens
viral infections
cold air
exercise
irritant dusts
vapours and fumes
emotion & drugs
17
Q

Pathophysiology: what happens to the SM, epithelial cells and the basement membrane?

A

SM - inappropriate + excessive contraction of SM. hypertrophy + proliferation of SMCs

Epithelial cells - may be abnormal, altered expression of matrix regulating proteins. neoplasia: increase in number of goblet cells

BM - increased thickening

18
Q

What makes the airway narrow?

A

SM contraction
thickening of the airway by cellular infiltration
secretions within the airway lumen

19
Q

Presentation

A

cough + chest tightness
diurnal variation
worse at nights and early morning
provoked by triggers

20
Q

Presentation during an attack

A

reduced chest expansion, prolonged expiratory time and bilateral polyphonic wheezing

21
Q

Diagnostic tests

A

Skin prick test
CXR- hyperinflation?

PaO2 and PaCO2 down –> hyperventilation

Variable airflow limitation
Diurnal variation of PEFR - increased after inhalation of bronchodilator (reversibility testing)

22
Q

How would you rule out bronchopulmonary aspergillosis ?

23
Q

which out of bronchodilators and steroids alleviate symptoms and which target inflammation?

A

BDs- alleviate Sx

steroids- target inflammation

24
Q

What’s step 1 for BTS stepwise treatment for asthma?

A

occasional SABA for symptom relief e.g. salbutamol

short acting beta-2 agonist

25
if SABA isn't sufficient, what Tx would you add?
standard-dose inhaled steroid e.g. beclometasone
26
when would you add salmeterol to Tx and review Dx?
its a LABA. would add to inhaled steroid and SABA (step 3)
27
What's step 4 for BTS stepwise treatment for asthma?
consider trials of high beclometasone (inhaled steroid)
28
If all else fails, whats the final step in Tx?
regular oral prednisolone
29
What's the molecular difference between SABAs and LABAs?
a LABA is a SABA with an added long lopophilic chain
30
how to B2-adrenoceptor agonists work?r
they relax bronchial smooth muscles (increasing cAMP), acting within minutes
31
Mx for a really severe asthma attack?
02 40-60%, salbutamol nebuliser, prednisolone